Presence and inducibility of peroxisomes in a human glioblastoma cell line

• Published in: Biochimica et biophysica acta 2000-05, Vol.1474 (3), p.397-409
• Main Authors: Cimini, A, Cristiano, L, Bernardo, A, Farioli-Vecchioli, S, Stefanini, S, Cerù, M.P
• Format: Article
• Language: English
• Subjects: Acyl-CoA Oxidase; Alitretinoin; Apoptosis; Brain Neoplasms; Catalase - analysis; Catalase - antagonists & inhibitors; Catalase cytochemistry; Cell Division - drug effects; Decanoic Acids - pharmacology; Flow Cytometry; Fluorocarbons - pharmacology; Glioblastoma; Humans; Immunoblotting; Microscopy, Phase-Contrast; Neuroectodermal cell line; Oxidoreductases - analysis; Perfluorodecanoic acid; Peroxisome proliferator; Peroxisome proliferator-activated receptor; Peroxisome Proliferators - pharmacology; Peroxisomes - enzymology; Peroxisomes - ultrastructure; Receptors, Cytoplasmic and Nuclear - analysis; Transcription Factors - analysis; Tretinoin - pharmacology; Tumor Cells, Cultured - drug effects; Tumor Cells, Cultured - ultrastructure
• ISSN: 0304-4165; 0006-3002; 1872-8006
• DOI: 10.1016/S0304-4165(00)00036-2

We investigated the effect of the peroxisomal proliferator (PP) perfluorodecanoic acid (PFDA), alone or in combination with 9- cis-retinoic acid (RX) on the human glioblastoma cell line Lipari (LI). Cell proliferation, apoptotic rate, peroxisome morphology and morphometry, peroxisomal enzyme activities and the presence of peroxisome proliferator-activated receptors (PPARs) were examined. We show that PFDA alone produces pleiotropic effects on LI cells and that RX enhances some of these effects. Peroxisomal number and relative volume, as well as palmitoyl-CoA oxidase activity and protein, are increased by PFDA treatment, with a synergistic effect by RX. The latter, alone or in association with PFDA, induces catalase activity and protein, increases apoptosis and decreases cell proliferation. PPAR isotypes α and γ were detected in LI cells. While the former is apparently unaffected by either treatment, the latter increases in response to PFDA, independent of the presence of RX. The results of this study are discussed in terms of PPARα activation and PPARγ induction by PFDA, by either a direct or an indirect mechanism.